Watch the mechanism of disease video to learn more about the underlying sources of ITP

Complex immune dysregulation leads to autoimmunity and inflammation1-4

In ITP, immune dysregulation lowers platelet counts through multiple pathways. Autoreactive B cells produce autoantibodies that target platelets for destruction by macrophages and impair megakaryocyte maturation, reducing platelet production. Autoantibodies may also destroy platelets through other mechanisms.2-4

Immune system activity can also lead to elevated levels of inflammatory markers.2-4

Adapted from Kashiwagi H, et al. Int J Hematol. 2013;98(1):24-33. © Japanese Society of Hematology (JSH)

Bruton’s tyrosine kinase (BTK) plays a critical role in complex immune dysregulation5,6

B cells are responsible for the production of autoantibodies: macrophages are essential for phagocytosis: and the NLRP3 inflammasome plays a key role in systemic inflammation. All of these processes are regulated by BTK.

In B cells: The BTK pathway is crucial for proliferation, differentiation, and autoantibody production

In macrophages: Various signaling pathways dependent on BTK drive phagocytosis, degranulation, and the production of inflammatory cytokines

Systemically: BTK drives the production of mediators of inflammation like NLRP3 inflammasome, which can contribute to platelet destruction and systemic inflammation

Ongoing research has found that patients living with ITP have elevated inflammatory markers, including6:

  • TNF-α and IFN-γ
  • IL-2 and IL-6
  • NLRP3 inflammasome cytokines IL-1β and IL-18

BTK is implicated in the production or activation of these inflammatory markers and is a critical driver of inflammation

IFN, interferon; IL, interleukin; NLRP3, nucleotide-binding domain, leucine-rich repeat and pyrin domain-containing protein 3; TNF, tumor necrosis factor.

Next: Patients need more treatment options

Learn about unmet needs in the current ITP treatment landscape.

Unmet Needs in ITP

    1. Kashiwagi H, Tomiyama Y. Pathophysiology and management of primary immune thrombocytopenia. Int J Hematol. 2013;98(1):24-33. 2. Andreescu M. The link between immune thrombocytopenia and the cytokine profile: a bridge to new therapeutical targets. Front Hematol. 2023;2:1191178. 3. Qiao J, Liu Y, Li X, et al. Elevated expression of NLRP3 in patients with immune thrombocytopenia. Immunol Res. 2016;64(2):431-437. 4. Schifferli A, Cavalli F, Godeau B, et al. Understanding immune thrombocytopenia: looking out of the box. Front Med (Lausanne). 2021;8:613192. 5. Zhu S, Gokhale S, Jung J, et al. Multifaceted immunomodulatory effects of the BTK inhibitors ibrutinib and acalabrutinib on different immune cell subsets - beyond B lymphocytes. Front Cell Dev Biol. 2021; 9:727531. 6. Neys SFH, Hendriks RW, Corneth OBJ. Targeting Bruton's tyrosine kinase in inflammatory and autoimmune pathologies. Front Cell Dev Biol. 2021;9:668131.